Deep Venous Pathology Eberhard Rabe Department of Dermatology University of Bonn Germany
Disclosures None for this presentation Consultant: Sigvaris, EUROCOM Speakers bureau: Bayer Vital, Aspen, Boehringer, Medi
CEAP Classification Clinical classes: Etiology: Anatomy: Physiopathology: C0 C6 Primary Secondary (Postthrombotic) Congenital Deep veins, Deep + Superficial veins, Deep + Superficial + Perforator Reflux Obstruction Reflux and Obstruction
Deep venous pathology Primary Reflux With or without varicose veins Obstruction May-Thurner Syndrome Secondary Reflux and / or Obstruction Postthrombotic Syndrome Congenital Reflux and / or Obstruction Angiodysplasia Reflux Congenital venous valve agenesia
Deep venous reflux may be due to the same genetic and vein wall changes as is responsible for the developement of VV Untreated VV may trigger the develpement of deep venous Dilatation and reflux Varicose veins
Deep venous axial reflux primary
Primary deep venous insufficiency in patients with VV W. Hach: Phlebologie 1980: The volume overload of the deep veins in patients with untreated GSV VV leads to dilatation, elongation and reflux in the popliteal and femoral veins. He called this secondary popliteal and femoral vein insufficiency due to VV
Deep venous insufficiency in VV Sales CM et al. Correction of lower extremity deep venous incompetence by ablation of superficial venous reflux. Ann Vasc Surg1996 Mar;10(2):186-9. 45 patients with GSV VV 17 (38 %) had reflux in the femoral vein After GSV ablation reflux vanished in 16/17 patients
Deep venous insufficiency in VV W. Stranzenbach, W. Hach, Phlebologie 1991 Diameter of the FV and PV before and 5 years after GSV ablation Femoral vein Popliteal vein Before GSV ablation 18,9 mm 16,5 mm 5 years follow-up 14,9 mm 14,7 mm
May-Thurner Syndrome From: Sarah Carroll, Stephan Moll Inferior Vena Cava Filters, May-Thurner Syndrome, and Vein Stents https://doi.org/10.1161/circulationaha.115.019944, Circulation. 2016;133:e383-e387
Unexpected positive effects of venous stenting in deep venous reflux patients Raju S, Darcey R, Neglen P: Unexpected major role for venous stenting in deep reflux disease. J Vasc Surg 2010; 51: 401-408 Prospective case series (11 Jahre) N= 504 patients, n= 528 legs Dilatation and stenting of iliac vein, single treatment CEAP classes C3 44% C4 + C5 27% C6 25% Etiology of obstruction 37% non-thrombotic 54% postthrombotic 9% combined 100% deep reflux 69% superficial reflux Results after 5 years 88% 54% 88% 78% 55% patency rate, secundary, cumulative healed ulcers no recurrence improvement of pain improvement of swelling 37
Dilatation-Stent Results Neglen and Raju
13 Pathophysiology of PTS Acute DVT: Thrombus + Inflammatory mediators + recanalisation Venous Obstruction Damage of venous valves (Reflux) Ambulatory venous hypertension Damaged microcirculation Capillary leak Venous dilatation, Swelling Pigmentation Induration Ulceration
Deep venous axial reflux PTS
Postthrombotic Syndrome Occlusion, obstruction Recanalisation Collaterals Valve destruction, Reflux
Deep venous pathology in PTS Saarinen et al. J Cardiovasc Surg 2000;4:441-6 prospektive, n=26, 20 Mon. follow-up 50% had reflux or obstruction in popliteal vein Saarinen et al. J Vasc Surg 2002;36:959-64 retrospektive, n=50, 8,4 Years follow-up After isolated lower leg DVT 40% had popliteal vein reflux
Postthrombotic Syndrome Franzeck et al. Thromb&Haemost 1997;77:1109-12 prospektive, n=39, 12 ye<rs follow-up Johnson et al. J Vasc Surg, 1995, 21, 307-12 retrospektive, n=78, 3 years follow-up Franzeck Johnson Obstruction 8,5% 15% Reflux 33% 18% Obs.+Reflux 50% 65%
Postthrombotic Syndrome Markel et al. Wiener Med Wschr 1994;144:216-20 prospektive, n=107/106 legs, 341 days follow-up t0 t7 t30 t365 0% Reflux 17% Reflux 37% Reflux 66% Reflux V.popl. 58%, V.fem. 37%, V.fem com. 33%, V.tib.post. 18%, GSV25%
Diagnosis of PTS No real gold standard Clear diagnosis of previous DVT Typical duplex findings No close correlation between reflux and clinical signs and symptoms Signs and symptoms typical for chronic venous insufficiency Villalta Score
Villalta PTS - Score 5 symptoms Pain Cramps Heaviness Itching Paresthesia 6 signs Edema Induration Pigmentation Venous ectasia Redness Pain during calf compression Additional parameter: venous leg ulcer
PTS Scale: Villalta Updated Score based on 5 symptoms and 6 signs (0 3 score points: 0=absent, 1=mild, 2=intermediate, 3=severe) Maximum Score: 33 Score 0-4 Score 5-9 Score 10-14 Score >14, or Ulcer = no PTS = mild PTS = moderate PTS = severe PTS Ulcus cruris has no score points elevates the score to a minimum of 15 The Scientific and Standardization Committee of the ISTH 2009 judged that the Villalta scale was the scale most suitable for defining the presence and severity of PTS after objectively diagnosed DVT Kahn and Ginsberg. Post Thrombotic Guidelines. TIGC, 2008
Villalta Scale Good tool to document and score signs and symptoms of PTS but Not specific for PTS CVI caused by varicose veins may have the same signs and symptoms High prevalence of combined VV and PTS Usually no baseline (pre-dvt) score or evaluation in the studies
PTS: (DVT fem V and pop V) VV: SSV and GSV
Prevalence of PTS Prevalence of PTS: 1 5% in general population Prevalence of CVI: 15 % Overlap of signs and symptoms possible Bonn Vein Study 2003 3072 participants, general population, 18-79 Y Prevalence PTS 1.1 % Men 0.9 % Women 1.2 % Prevalence of CVI (C 3 C 6 ): 17 %
Incidence of PTS Early studies (from Prandoni & Kahn BJH 2009) 20 100 % after 4 10 years (Bauer, 1942, Gjores 1956) Recent studies Overall 50 % up to 2 years after first DVT (Kahn 2004) Up to 10 % severe PTS
Susan Kahn et al: Compression stockings to prevent postthrombotic syndrome: a randomised placebo-controlled trial. The Lancet 2014; 383: 880-888 Primary outcome Number of post-thrombotic syndrome events as assessed by Ginsberg's criteria (cumulative incidence) Secondary outcomes Number of post-thrombotic syndrome events as assessed by Villalta's criteria (cumulative incidence) Villalta severity category Active stockings (n=409) Placebo stockings (n=394) Hazard ratio * (95% CI) 44 (14 2%) 37 (12 7%) 1 13 (0 73 1 76) 176 (52 6%) 168 (52 3%) 1 00 (0 81 1 24) None (score <5) 185 (51 3%) 178 (51 4%) Mild (5 9) 119 (33 0%) 111 (32 1%) Moderate (10 14) 30 (8 3%) 37 (10 7%) Severe (>14 or ulcer) 27 (7 5%) 20 (5 8%)
V Hach-Wunderle, R Bauersachs, H Gerlach, S Eberle, S Schellong, H Riess, H Carnarius, E Rabe: Post-thrombotic syndrome 3 years after deep venous thrombosis in the Thrombosis and Pulmonary Embolism in Out-Patients (TULIPA) PLUS Registry. J Vasc Surg: Venous and Lym Dis 2013;1:5-12 Variable TULIPA TULIPA PLUS No VV, CVI, or DVT VV, CVI, or DVT P (DVT subgp) before index thrombosis (n=1388) (n=275) (n=135) (n=140) History of DVT 91 (29.4) 0 (0.0) 82 (58.6) VV 96 (31.0) 0 (0.0) 90 (64.3) CVI 38 (12.3) 0 (0.0) 34 (24.3) No PTS 179 (65.1) 102 (75.6) 77 (55.0) PTS 96 (34.9) 33 (24.5) 63 (45.0) Mild 65 (23.6) 23 (17.0) 42 (30.0) 0.004 Moderate 22 (8.0) 8 (6.0) 14 (10.0) Severe 9 (3.3) 2 (1.5) 7 (5.0)
Tulipa registry: Villalta score for PTS severity at 3-year follow-up by index-dvt extension [PTS Incidence Population*] Villalta score All patients (n=135)* N, % (95% CI) Proximal (n=71)* N, % (95% CI) Distal (n=64)* N, % (95% CI) p No PTS 102, 75.6 (68.3-82.8) 48, 67.6 (56.7-78.5) 54, 84.4 (75.5-93.3) 0.032 Mild to moderate PTS Severe PTS 31, 23.0 (15.9-30.1) 2, 1.5 (0.2-5.3) 22, 31.0 (20.2-41.7) 1, 1.4 (0.04-7.6) 9, 14.1 (5.6-22.6) 1, 1.6 (0.04-8.4) * Patients who had a personal history of DVT or showed any sign of varicose veins or CVI at day 1 are excluded
Klippel Trénaunay Syndrome
Angiodysplasia - Epidemiology - Incidence overall 1% Predominantly venous 64% Predominantly in periphery
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